STUDIES IN EDEMA. IV. WATER RETENTION AND THE ANTI-DIURETIC HORMONE IN HEPATIC AND CARDIAC DISEASE 12
Open Access
- 1 October 1953
- journal article
- research article
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 32 (10) , 931-939
- https://doi.org/10.1172/jci102818
Abstract
An infusion of 5% glucose in water was administered intraven. at 10 cc./ minute to 7 control subjects, 10 cardiacs, and 5 patients with liver disease (4 with decompensated liver cirrhosis and 1 with infectious hepatitis), and the resulting water diuresis studied. While the glucose infusion continued and after the urine flow reached a plateau, 0.57 mU./kg. of Pitressin was injd. intraven. into the 7 controls, into 6 of the cardiac patients, and into the 5 hepatic patients. Following onset of the infusion the avg. time required for attainment of peak diuresis in the control subjects, cardiac patients, and liver patients was : 85.1[plus or minus]32.3, 99.1 [plus or minus] 32.1, and 88.6[plus or minus] 27.2 min., respectively. The avg. peak urine flows attained during the hydration periods were: 12.0[plus or minus].2.7, 6.7[plus or minus]3.3, and 11.9[plus or minus] 3.0 cc./min. for the 3 groups. There was no significant difference in the duration of, and intensity of, Pitressin anti-diuresis under these exptl. conditions in 3 groups of patients, except for 2 of the cardiacs who demonstrated an enhanced water antidiuresis. In the dosage administered, Pitressin did not exert any significant effect on the urinary output of Na, chloride, or K. As for the effect of Pitressin on the concns. of electrolytes in the serum, the only consistent change noted was that of the serum Na which tended to fall during Pitressin antidiuresis in the 5 patients with liver disease. The 2 cardiac patients who showed the augmented Pitressin effect also had the lowest concns. of serum Na (121.9 and 130 m.eq./l.), but a causal relationship remains to be established. These data offer no conclusive evidence for any deficiency in the mechanisms of inactivation of Pitressin administered in physiological dosage to controls, cardiacs, or patients with liver disease.Keywords
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